We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
APOBEC3G targets human T-cell leukemia virus type 1.
- Authors
Sasada, Amane; Takaori-Kondo, Akifumi; Shirakawa, Kotaro; Kobayashi, Masayuki; Abudu, Aierkin; Hishizawa, Masakatsu; Imada, Kazunori; Tanaka, Yuetsu; Uchiyama, Takashi
- Abstract
Background: Apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) is a host cellular protein with a broad antiviral activity. It inhibits infectivitiy of a wide variety of retroviruses by deaminating deoxycytidine (dC) into deoxyuridine (dU) in newly synthesized minus strand DNA, resulting in G-to-A hypermutation of the viral plus strand DNA. To clarify the mechanism of its function, we have examined the antiviral activity of APOBEC3G on human T-cell leukemia virus type 1 (HTLV-1), the first identified human retrovirus. Results: In this study, we have demonstrated that overexpressed as well as endogenous APOBEC3G were incorporated into HTLV-1 virions and that APOBEC3G inhibited the infection of HTLV-1. Interestingly, several inactive mutants of APOBEC3G also inhibited HTLV-1 and no Gto-A hypermutation was induced by APOBEC3G in HTLV-1 genome. Furthermore, we introduced the human immunodeficiency virus type 1 (HIV-1) vif gene into HTLV-1 producing cell line, MT-2, to antagonize APOBEC3G by reducing its intracellular expression and virion incorporation, which resulted in upregulation of the infectivity of produced viruses. Conclusion: APOBEC3G is incorporated into HTLV-1 virions and inhibits the infection of HTLV-1 without exerting its cytidine deaminase activity. These results suggest that APOBEC3G might act on HTLV-1 through different mechanisms from that on HIV-1 and contribute to the unique features of HTLV-1 infection and transmission.
- Subjects
APOLIPOPROTEIN B; ADULT T-cell leukemia; RETROVIRUSES; HTLV diseases; HIV; MESSENGER RNA
- Publication
Retrovirology, 2005, Vol 2, p32
- ISSN
1742-4690
- Publication type
Article
- DOI
10.1186/1742-4690-2-32